普洱茶通过降低NF-κB活性促巨噬细胞凋亡改善动脉粥样硬化

Objective: To explore the anti-atherosclerosis mechanism of pu-erh tea by reducing the expression and activity of NF-κB and promoting macrophage apoptosis. Methods: ① ApoE^-/- mice were fed with pu-erh tea extract for 8 and 16 weeks to observe the positive rate of CD68 and the area of lipid plaque. ② Apoptosis detection kit was used to detect the apoptosis of macrophages. ③ P65 and IkB-β expressions in aortic plaque and macrophages were detected by Real-time quantitative PCR and Western blot; the expressions of inflammatory factors in aortic plaque were detected. ④ Electrophoretic mobility change assay (EMSA) was used to analyze the binding activity of NF-κB DNA. Results: ① The area fraction of lipid plaque in ApoE^-/- mice in the 16-week intervention group was significantly reduced (vs. control group, P<0.05). The area of lipid components in the 16-week intervention group was significantly reduced (vs. control group, P<0.05). ② The positive rate of CD68 in the plaque was significantly lower in the 8-week and 16-week intervention group than in the control group (vs. control group, P<0.05). The apoptosis rate of macrophages in aortic plaque (vs. control group, P<0.05). ③ The expressions of p65 gene and protein in macrophages of pu-erh tea extract intervention group 8 and 16 weeks decreased (vs. control group, P<0.05). The expressions of I-κBβ gene and protein in 16-week intervention group decreased (vs. control group, P<0.05). The relative expression levels of IL-6, IL-12 and TNF-α in aorta tissue of 16-week intervention group decreased compared with control group (vs. control group, all P<0.05). There was no significant difference in the expressions of IL-8, IL-18, MMP9, ICAM and VCAM between the two groups (vs. control group, all P>0.05). ④ The average gray value of NF-κB DNA binding activity in the 8- and 16-week intervention groups decreased respectively (vs. control group, P<0.05). Conclusion: Pu-erh tea may play an anti-atherosclerosis role by inhibiting the expression and activity of NF-κB, promoting the apoptosis of macrophages and reducing the level of inflammation in vivo. This mechanism may not be mediated by I κB.